SIRT3/6/7: promising therapeutic targets for pulmonary fibrosis

Pingping Huang; Dan Qin; Yanling Qin; Sha Tao; Guangnan Liu

doi:10.3389/fcell.2025.1557384

SIRT3/6/7: promising therapeutic targets for pulmonary fibrosis

Front Cell Dev Biol. 2025 Apr 2:13:1557384. doi: 10.3389/fcell.2025.1557384. eCollection 2025.

Authors

Pingping Huang^#¹, Dan Qin^#², Yanling Qin¹, Sha Tao¹, Guangnan Liu¹

Affiliations

¹ Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Guangxi Medical University, Nanning, China.
² Department of Endocrinology, The Second Affiliated Hospital of Guangxi Medical University, Nanning, China.

^# Contributed equally.

Abstract

Pulmonary fibrosis is a chronic progressive fibrosing interstitial lung disease of unknown cause, characterized by excessive deposition of extracellular matrix, leading to irreversible decline in lung function and ultimately death due to respiratory failure and multiple complications. The Sirtuin family is a group of nicotinamide adenine dinucleotide (NAD+) -dependent histone deacetylases, including SIRT1 to SIRT7. They are involved in various biological processes such as protein synthesis, metabolism, cell stress, inflammation, aging and fibrosis through deacetylation. This article reviews the complex molecular mechanisms of the poorly studied SIRT3, SIRT6, and SIRT7 subtypes in lung fibrosis and the latest research progress in targeting them to treat lung fibrosis.

Keywords: EMT; inflammation; mechanism; pulmonary fibrosis; signaling pathways; sirtuins.

Publication types

Review